Identification of novel mast cell genes by serial analysis of gene expression in cord blood-derived mast cells

AbstractThe gene expression profile of human cord blood-derived mast cells (MCs) was investigated using serial analysis of gene expression (SAGE). A total of 22 914 tags, representing 9181 unique transcripts, were sequenced. By selecting tags that were detected more frequently in MCs than in other tissues, genes characteristic of MCs were enriched. Reverse transcription-PCR and the high-density oligonucleotide array hybridization confirmed the validity of our SAGE result. About 70% of the selected genes were previously uncharacterized. Northern blot analysis showed the MC-specific expression of selected genes. This inventory will be useful to identify novel genes with important functions in MCs

Spectroscopic study on deuterated benzenes. I. Microwave spectra and molecular structure in the ground state.

We observed microwave absorption spectra of some deuterated benzenes and accurately determined therotational constants of all H/D isotopomers in the ground vibrational state. Using synthetic analysis assuming that all bond angles are 120°, the mean bond lengths were obtained to be r[0](C–C) = 1.3971 Å and r[0](C–H) =r[0](C–D) = 1.0805 Å. It has been concluded that the effect of deuterium substitution on the molecular structureis negligibly small and that the mean bond lengths of C–H and C–D are identical unlike small aliphatic hydrocarbons, in which r[0](C–D) is about 5 mÅ shorter than r[0](C–H). It is considered that anharmonicity is very small in the C–H stretching vibration of aromatic hydrocarbons

Toll-like receptor 3 ligand specifically induced bronchial epithelial cell death in caspase dependent manner and functionally upregulated Fas expression

Background: Viral infections are the most common cause of asthma exacerbation. Virally infected epithelial cells undergo apoptosis. Although in healthy conditions, apoptosis may have a host-defensive role in limiting virus spread, this process may have a detrimental effect on damaged epithelium in asthma. Toll-like receptors (TLRs) are the receptors for various pathogens, and viruses possess several components that can activate TLR3, TLR4, and TLR7/8. However, as it has not been determined as to which component is responsible for virus-induced epithelial cell apoptosis, we comprehensively analyzed the effects of all TLR ligands on apoptosis. Methods: BEAS-2B cells or primary cultured human bronchial epithelial cells (PBECs) were stimulated by TLR 2, 3, 4, 5, 7/8, and 9 ligands and cell death was analyzed by flow cytometry. Chemokine generations induced by these ligands were also analyzed. Results: The TLR3 ligand polyinosinic–polycytidylic acid (poly I:C) specifically induced chemokine generation and apoptosis, while other TLR ligands including those for TLR5, 7/8, and 9 had no effect. The response to poly I:C had two phases, which included rapid secretion of chemokines and subsequent apoptosis in a later phase. Poly I:C induced apoptosis in a caspase-dependent manner and functionally upregulated the expression of Fas. Conclusions: Previous findings indicating that viruses induced caspase-dependent death and upregulated Fas expression were reproduced by poly I:C, suggesting the central role of dsRNA/TLR3 in virus-induced apoptosis. Since these processes may have detrimental effects on pre-existing epithelial damage, the dsRNA/TLR3 pathway may be potential novel treatment target for virus-induced exacerbation of asthma